Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatopathy associated with glucocorticoid therapy or with naturally occurring hyperadrenocorticism was detected retrospectively in hepatic biopsy specimens from 22 of 60 dogs, by histologic review. The hepatopathy was characterized by centrilobular vacuolization, perivacuolar glycogen accumulation within hepatocytes, and focal centrilobular necrosis. The predominant clinical findings were hepatomegaly, increased serum enzyme activity associated with hepatic disease, and increased bromsulphalein retention. The hepatopathy appeared to be reversible.
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PMID:A retrospective study of probable glucocorticoid-induced hepatopathy in dogs. 84 10

A study of liver abnormalities in 36 patients with mixed cryoglobulinemia in the absence of underlying infectious, connective tissue, or lymphoproliferative disorders revealed clinical or biochemical evidence of liver dysfunction in 84%. Hepatomegaly was detected in 77%, splenomegaly in 54%, and abnormalities in bilirubin, alkaline phosphatase, or serum glutamic oxalacetic transaminase in 77%. Only four of the patients had overt liver disease. Of 15 biopsies from 12 patients, there was normal tissue structure in two, minimal nonspecific changes in one, portal fibrosis in three, chronic persistent hepatitis in one, chronic active hepatitis in two, chronic active hepatitis with cirrhosis in four, and postnecrotic cirrhosis in two. These findings, together with the previously reported high incidence of serologic evidence of hepatitis B virus (HBV) infection, support the view that the syndrome of purpura, arthritis, and nephritis is often a consequence of immune-complex vasculitis secondary to HBV infection.
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PMID:Liver involvement in the syndrome of mixed cryoglobulinemia. 90 Jun 72

Clinicians should not minimize or overlook the importance of percussion of the liver and the spleen and of auscultation over the liver as routine parts of abdominal examination. Splenic percussion can be used to detect splenomegaly even before the spleen becomes palpable. The span of liver dullness on percussion can be compared with established normal standards to detect hepatomegaly or alterations caused by cirrhosis. A systolic bruit, a friction rub, or a venous hum detected by auscultation over the liver is an important sign of liver disease.
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PMID:Abdominal examination: role of percussion and auscultation. 92 43

Sixteen cases of chronic Q fever are described. In eight there was a history of exposure to infection from farms or farm products. All had valvular heart disease, involving the mitral valve in nine and the aortic valve in seven. Infection occurred on a prosthetic valve in two patients. Arterial embolism was common. Venous thrombosis occured in three patients, and pulmonary embolism occurred in three other patients. Complement fixing antibodies to phase 1 antigen were found in a titre of 1:200 or greater in all except two patients. In one of these post-mortem examination revealed rickettsial bodies in mitral valve vegetations, and in the other Coxiella burneti was isolated from heart valve tissue. The majority presented with infective endocarditis but two presented primarily with liver disease. All patients had evidence of liver involvement and in one this led to death from cirrhosis. Abnormal tests of liver function, particularly hyperglobulinaemia, raised alkaline phsophatase and abnormal bromsulphthalein retention were found in all patients. Hepatic histology was abnormal in all eight patients in whom it was studied. The commonest features were mononuclear cell infiltration of the portal tracts and prominence of the sinusoidal Kupffer cells. Patchy focal necrosis of parenchymal cells, granulomata, fatty change, and eosinophilia of the sinusoidal walls were also noted in several patients and cirrhosis developed in one. Six patients had a purpuric rash, and in 12 there was thrombocytopenia. It is suggested that the presence of hepatomegaly and liver involvement and thrombocytopenia may help to differentiate Q fever endocarditis from bacterial endocarditis. Raised serum IgM and IgA levels occured frequently, but with only a moderate dominance of IgM. Sheep cell agglutination and latex fixation tests for rheumatoid factor were occasionally positive. Several features of the disease suggest the possibility that immune-complex mechanisms may play a role in chronic Q fever. Treatment was with prolonged courses of tetracycline usually combined with lincomycin. Seven patients underwent valve replacement surgery for haemodynamic reasons. Five patients died; two from heart failure, one from cirrhosis, one seven days after valve replacement and one from intraperitoneal haemorrhage following percutaneous liver biopsy. Three patients have survived for more than five years, and another six for more than three and a half years after diagnosis. Of these nine patients, three received medical therapy alone and six required valve replacement as well. Antibiotics have been discontinued in four patients who have had valve surgery and three others. Six patients had received antibiotics for continuous periods varying from 29-62 months. In the period after stopping therapy varying from 15-21 months, no relapse has occured. A seventh patient, who had received antibiotics for four months prior to valve replacement, has survived 43 months after the withdrawal of antibiotics...
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PMID:Chronic Q fever. 94 Sep 18

Liver disease in children with alpha1-antitrypsin deficiency and protease inhibitor type ZZ does not necessarily carry a bad prognosis. Fourteen of our 18 patients presented with the neonatal hepatitis syndrome and four had hepatomegaly without jaundice. Although four patients have died of cirrhosis and its complications, and three have severe liver disease, most of the 11 others, of whom four are over 13 years of age, have relatively little clinical, biochemical, or histologic evidence of liver disease. Persistent elevation of SGOT during the third year of life and renal or pulmonary problems were associated with a poor prognosis. Liver biopsy early in the course of the disease was not helpful prognostically but was useful in assessment of the severity of liver disease and demonstration of alpha1AT storage, alpha1AT deficiency was found in 29% of our patients who presented with the neonatal hepatitis syndrome. One of seven apparently healthy Pi type ZZ sibs of our patients had significant liver disease which had not been suspected previously.
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PMID:Liver disease associated with alpha1-antitrypsin deficiency in childhood. 108 17

Among 424 children with liver disease, 20 had alpha1-antitrypsin deficiency associated with protease inhibitor ZZ phenotype. This disorder manifested itself as cholestasis in early infancy in 19 children. Jaundice and pruritus cleared in 16 of these by 7 months of age, but hepatomegaly and laboratory evidence of mild hepatic dysfunction persisted in all. Biliary cirrhosis and portal hypertension eventually developed or was suspected in eight, and hypoplasia of intraheptic bile ducts was demonstrated in another four. Routine screening revealed intermediate alpha1-antitrypsin deficiency in 16 other children with various types of liver disease. The phenotype in these patients was MZ, MS, or SZ. PAS-positive granules were present in liver of all patients with the ZZ phenotype and in none with other phenotypes. The findings indicate that manifestations and prognosis of this inherited liver disease are extremely variable.
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PMID:Alpha1-antitrypsin deficiency and liver disease in children: phenotypes, manifestations, and prognosis. 108 71

This report describes the clinical, biochemical, and hepatic morphologic findings in ten children with severe serum alpha1-antitrypsin deficiency. Genetic protease inhibitor (Pi) phenotyping, using acid-starch gel and crossed antigen-antibody electrophoresis, demonstrated Pi phenotype ZZ in all our cases. In eight patients, manifestations of liver disease appeared during the first year of life. The case reports show that alpha1-antitrypsin deficiency should be suspected in any child with neonatal hepatitis, unexplained hepatomegaly or splenomegaly, or cirrhosis. In our report, one infant is normal at age 6 months, and one infant had progressive hepatic damage that culminated in liver failure and death at age 6 months. The variable clinical course and prognosis for infants with severe alpha1-antitrypsin deficiency is well illustrated by these two infants.
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PMID:alpha1-Antitrypsin deficiency and liver disease in children. 108 88

In a study of fifty patients subjected to cardiac surgery nine (18%) had immediate post-operative liver complications. These included persistente jaundice, an increase in hepatomegaly and elevation of the alkaline phosphatase. In these and the rest of the cases there were extra-hepatic complications such as hyposystole, infarct, the post-pericardiotomy syndrome as related to the heart. Pulmonary complications were of infectious nature and a general complication was sepsis. These complications were sufficiently important to relate them etiologically to the hepatic disorder. Especially important is right hyposystole and it or tricuspid insufficiency can be blamed for the hepatic disorder in some of these patient. Nonetheless, these hepatic complications are seen less frequently now that we are giving effective treatment to the tricuspid insufficiency during the surgical intervention. We observed the clinical picture known as "benign postoperative cholestasis" in only two patients. Hepatitis with jaundice was seen in four patients during one to three months postoperatively. This was HB hepatitis and its course was more prolonged than that usually seen in Mexico, and it turned into chronic hepatitis in four patients. Biopsies done in one case a six months and in the other at nine months post-operatively showed the picture of chronic aggresive hepatitis. In those patients who did not have hepatic complications a late liver evaluation showed an improvement as compared to the pre-operative condition which was parallel to the hemodynamic improvement.
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PMID:[Hepatic complications in the postoperative of cardiac surgery]. 123 73

Two siblings with marked dwarfism, now 11 and 19 years of age, have been followed from infancy. The girl had frequent episodes of pneumonitis and presented at age 4 years with hepatic enlargement and ascites which proved to be due to constrictive pericarditis. The boy presented with growth failure and pseudohydrocephalus. He had fibrous dysplasia of the tibia and a pathologic fracture; acute hepatic congestion followed physical activity at age 13 years and led to the diagnosis of constrictive pericarditis. Muscle function was normal, there was no evidence for a primary liver disorder, and mental development was normal so that the coined word "mulibray" seemed inappropriate. Pericardiectomy produced only partial improvement; both patients have hepatic enlargement and continue to need diuretics. A third patient with dwarfism, frequent respiratory infections, and pericardial calcification has certain features of the syndrome.
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PMID:Constrictive pericarditis with dwarfism in two siblings (mulibrey nanism). 125 13

Symptomatic occlusion of hepatic veins, the Budd-Chiari syndrome (BCS), may be on the increase in women taking oral contraceptives. 17 liver scans in 7 patients with confirmed BCS over a 7-year period were studied. 6 of the 7 patients were women. When more than 1 vein is occluded BCS results, with hepatomegaly, abdominal pain, ascites, and hepatic histology showing centrizonal sinusoidal distention, hemorrhage, and necrosis. Mortality has been high. BCS is associated with polycythemia, oral contraceptive use, malignancy, trauma, and congenital abnormalities. The scintigram appearance with radiocolloid is usually characteristic but a similar appearance has rarely been reported in cirrhosis of the liver and in 1 case of contrictive pericarditis. Excessive uptake in the midline with markedly diminished activity at the periphery may be the 1st clue that BCS is present. Confusing conditions with incomplete BCS include partial hepatectomy, radiation injury, fortuitous segmental involvement by diffuse or focal liver disease, and rarely hepatic artery occlusion. Treatment is by the porto-caval shunting operation. Venous obstruction as shown venographically has had good correlation with liver scans. After the shunt procedure, hepatic artery flow to the affected lobes has increased as the pressure falls and underperfusion of the hypertorphied midline section. After 14 months, the midline area has shown no uptake, possibly because of atrophy. Radiocolloid uptake also appears in the ribs, spine, and lung. This uptake recedes when the liver function improves.
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PMID:Liver scan in Budd-Chiari syndrome. 126 39


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